Hypothyroidism develops when your thyroid gland can’t produce enough hormones to meet your body’s needs. The most common cause by far is an autoimmune attack on the thyroid, but surgery, radiation, medications, iodine deficiency, and problems with the pituitary gland can all trigger it too. Some people are born with it, and others develop it after pregnancy.
Autoimmune Disease: The Leading Cause
In countries with adequate iodine intake, an autoimmune condition called Hashimoto’s disease is responsible for most cases of hypothyroidism. Your immune system produces antibodies that attack the thyroid gland, and over time, large numbers of white blood cells build up in the tissue. This gradually damages the gland until it can no longer make enough thyroid hormones. Most people with Hashimoto’s test positive for thyroid peroxidase antibodies (TPO), which are markers of this immune attack.
The destruction happens slowly. You can have Hashimoto’s for years before your thyroid hormone levels drop low enough to cause symptoms. This is why many people don’t realize anything is wrong until routine blood work picks up an elevated TSH level, the signal your brain sends when it’s trying to push a struggling thyroid to work harder.
Surgery and Radiation Treatment
Having part or all of your thyroid removed (for cancer, nodules, or an overactive thyroid) is one of the most straightforward paths to hypothyroidism. If the entire gland is removed, you will need thyroid hormone replacement for life. Partial removal may or may not leave enough functioning tissue to keep hormone levels normal.
Radioactive iodine therapy, commonly used for Graves’ disease and toxic thyroid nodules, also destroys thyroid tissue. For people treated for Graves’ disease, the rate of hypothyroidism runs between 5% and 50% in the first year alone, with an additional 3% to 5% developing it each year afterward. Patients treated for a single toxic nodule fare better, with fewer than 10% developing permanent hypothyroidism even over long follow-up. Toxic multinodular goiter falls somewhere in between, with hypothyroidism rates ranging from about 20% to 75% within eight years depending on the radiation dose used.
Radiation therapy aimed at cancers of the head, neck, or brain can also damage the thyroid or the pituitary gland. Hypothyroidism has been reported in 20% to 50% of patients who received radiation for tumors near the sinuses or throat, and in roughly 65% of those irradiated for brain tumors.
Medications That Interfere With Thyroid Function
Several prescription drugs can cause hypothyroidism as a side effect. Lithium, widely used for bipolar disorder, causes hypothyroidism in up to 20% of patients by blocking the thyroid’s ability to release its hormones. Amiodarone, a heart rhythm medication, affects 14% to 18% of the people who take it. A single 200 mg tablet of amiodarone delivers 45 times the recommended daily intake of iodine, and that iodine flood can shut down hormone production in susceptible individuals.
Newer cancer immunotherapy drugs (checkpoint inhibitors) can also trigger thyroid inflammation that leads to permanent underactivity. Every step in your body’s process of making, releasing, transporting, and using thyroid hormones is vulnerable to drug interference, so if you develop symptoms of hypothyroidism after starting a new medication, your thyroid levels are worth checking.
Iodine Deficiency
Your thyroid needs iodine to build its hormones. Adults require about 150 micrograms per day, roughly the amount in half a teaspoon of iodized salt. Pregnant women need more, around 220 to 250 micrograms daily. If iodine intake drops below about 10 to 20 micrograms per day, hypothyroidism develops, often accompanied by a visible swelling of the thyroid called a goiter. The enlarged gland is the body’s attempt to trap more iodine from the bloodstream.
Iodine deficiency is rare in countries where salt is iodized, but it remains a significant problem in parts of the developing world. The consequences are especially severe during pregnancy: chronic, severe deficiency in utero can cause permanent intellectual disability, stunted growth, hearing loss, and other developmental problems in the child. Even mild to moderate deficiency in adults can impair mental function and work productivity.
Pituitary and Brain-Related Causes
Sometimes the thyroid itself is perfectly healthy, but it never gets the signal to produce hormones. That signal comes from the pituitary gland, a pea-sized structure at the base of the brain that releases TSH (thyroid-stimulating hormone). If the pituitary is damaged or compressed, TSH production drops and the thyroid idles.
The most common cause of this “central” hypothyroidism is a pituitary tumor, particularly large nonfunctioning adenomas or tumors that secrete growth hormone or prolactin. These account for more than half of acquired cases. Traumatic brain injuries and strokes (including subarachnoid hemorrhages) are increasingly recognized causes as well. In some of these cases, the pituitary still releases a version of TSH, but the molecule is structurally altered and can’t properly activate the thyroid. This makes the condition tricky to diagnose on standard blood tests, since TSH levels may look normal or only mildly low even though the hormone isn’t doing its job.
Pregnancy and Postpartum Thyroiditis
Pregnancy places heavy demands on the thyroid, and about 5% to 10% of women develop thyroid inflammation in the months after delivery. Postpartum thyroiditis typically follows a predictable pattern: a brief phase of overactivity as stored hormones leak from the inflamed gland, followed by a longer phase of underactivity as the damaged tissue struggles to keep up.
The condition usually resolves on its own within 12 to 18 months. Between 70% and 80% of women eventually recover full thyroid function and can stop any medication they started. The remaining 20% to 30% stay hypothyroid permanently and need long-term hormone replacement. Women who have had postpartum thyroiditis once are at higher risk of developing it again with future pregnancies, and they carry a higher lifetime risk of permanent hypothyroidism.
Congenital Hypothyroidism
Over a thousand babies are born each year in the United States with hypothyroidism. In 80% to 85% of cases, the cause is a thyroid gland that simply didn’t develop properly during fetal growth, either forming in the wrong location, growing too small, or not forming at all. Newborn screening catches these cases within days of birth, which is critical because untreated congenital hypothyroidism causes irreversible developmental delays. With early treatment, most of these children develop normally.
Who Is Most at Risk
Hypothyroidism is far more common in women than in men, and the gap widens with age. Treatment data from national health surveys show that among people aged 18 to 44 with hypothyroidism, the gender difference is relatively modest. By age 60 and older, over 90% of women with the condition are on treatment compared to about 66% of men, reflecting both higher prevalence in women and a pattern of underdiagnosis in men.
Your risk also rises if you have a family history of thyroid disease, if you already have another autoimmune condition (like type 1 diabetes, celiac disease, or rheumatoid arthritis), or if you’ve had radiation to your head or neck. Age itself is a significant factor. TSH levels tend to drift upward as people get older, and the prevalence of both overt and subclinical hypothyroidism climbs steadily past middle age.
How It Gets Diagnosed
A simple blood test measuring TSH is the primary screening tool. Normal TSH generally falls between about 0.45 and 4.12 mIU/L. When TSH rises above that range, it means your pituitary is working harder to push a sluggish thyroid. Mildly elevated TSH (roughly 4.5 to 9.9 mIU/L) is considered subclinical hypothyroidism, meaning your thyroid is underperforming but hasn’t fully failed yet. Even at this stage, it can contribute to cholesterol changes, blood pressure shifts, and reduced heart function, particularly in younger and middle-aged adults.
TSH at or above 10 mIU/L is the threshold where most guidelines recommend starting treatment, as levels this high are linked to increased risk of heart disease and heart failure. Your doctor will typically also measure free T4 (the main thyroid hormone circulating in your blood) to confirm the diagnosis and gauge severity. If autoimmune disease is suspected, a TPO antibody test can confirm Hashimoto’s as the underlying cause.